The invention relates to “active implantable medical devices” as defined by Directive 90/385/EEC of 20 Jun. 1990 of the Council of the European Communities, specifically implants to continuously monitor heart rhythm and deliver if necessary electrical pulses to the heart for stimulation, resynchronization and/or defibrillation in case of rhythm disorder detected by the device. It more particularly relates to devices for treating heart failure (HF), as an alternative or in addition to the treatment of cardiac rhythm disorders.
This therapy is designed to resynchronize the contraction of the heart chambers (atrium and ventricle) so as to improve the patient's condition by optimizing the phases of the hemodynamic cycle. The cycle includes pre-ejection, isovolumetric contraction, systolic ejection, isovolumetric relaxation and finally filling of the cavity.
Most of these devices implement a technique called “CRT” (Cardiac Resynchronization Therapy) or “BVP” (Bi-Ventricular Pacing) for delivering, as necessary, electrical pulses needed to ensure joint and continuous stimulation of the two (left and right) ventricles to resynchronize them. This biventricular resynchronization technique however addresses only one of the forms of heart failure, known as “systolic failure”. In this form of the disease, the heart muscle is unable to provide the force necessary to ensure adequate cardiac output, and the patient shows signs of expansion resulting in a delay of left ventricular depolarization. CRT biventricular pacing is then used to resynchronize the ventricles and make more uniform cardiac contraction.
In the other form of heart failure called “diastolic failure” or “preserved ejection fraction heart failure” (HFpEF, Heart Failure with preserved Ejection Fraction), there is no desynchronization of the ventricles; it comes from a failure in the left ventricular filling. Biventricular CRT stimulation will be ineffective in this case. This condition affects about 40% of heart failure patients, and there is no known effective treatment to remedy to it.
This form of disease in some patients may be the result of a disorder of conduction in the atria (inter-atrial block), which delays the depolarization, and therefore the contraction of the left atrium (OG) with respect to the right atrium (OD). However, as atrioventricular conduction pathways are not altered, depolarization and contraction of the right (VD) and left (VG) ventricles occur within a reasonable time, without synchronization VD-VG. It is between the contraction of the left atrium and that of the left ventricle that the inter-atrial block OD-OG generates a poor sequencing OG-VG. The delay of the contraction of the left atrium has for consequence that it contracts substantially at the same moment as the left ventricle, and therefore cannot properly fulfill its function and contribute to the left ventricular active filling.
To treat this heart failure with preserved ejection fraction, a technique of atrial overdriving, pathology, has been proposed. This is described for example in the U.S. Pat. No. 7,494,921B1, which describes permanently stimulating the left atrium to a frequency slightly above the spontaneous sinus rhythm frequency (i.e. the rate of the right atrium), thereby systematically causing premature depolarization of the left atrium and restoring an almost normal OG-VG sequence.
Specifically, in this technique, the device regularly measures the spontaneous rhythm of the patient and applies a sequence of pacing pulses at a slightly faster rate, arbitrarily programmed to cause a prematurity in the order of 50 to 100 ms compared to an atrial coupling interval corresponding to the spontaneous sinus rhythm. After several cycles at this accelerated pace, the frequency gradually slows until reappearance of spontaneous activity, then the overdriving method is repeated in the same way.
In the description of this technique, the “atrial coupling interval” or “atrial coupling” is defined as the time interval separating two spontaneous (in sinus rhythm, also designated as “PP interval”) or stimulated consecutive atrial events. The applied stimulation frequency thus varies continuously between values wherein it is too fast (overdriving period) or too slow (period of reappearance of spontaneous rhythm, with OD-VD synchronization), without real monitoring of the effectiveness of a possible return to a proper synchronization of the left cavities.
It should also be noted that this pacing mode may interfere with the filling of the right cavities. In fact, due to premature stimulation of the left atrium, the OD-VD synchronization is significantly altered in a manner which may be incompatible with satisfactory filling of the right ventricle (we will clarify these aspects in the detailed description). Improvement therapy in left ventricular filling is thus likely to induce adverse effects on the filling of the right ventricle, so in the cavity that was not affected by the pathology to be treated.
Moreover, this technique requires the presence of a right ventricular sensing lead, so as to ensure that overdriving is controlled on the basis of the actual atrial activity, and not on signals detected at the atrium but actually due to the depolarization of the ventricles (far-field signals).
Another technique is described in EP 2471575 A1 (Sorin CRM SAS) which implements a sensor for collecting an endocardial acceleration signal (EA). The EA signal is analyzed to detect the presence of a specific component reflecting atrial contraction (EA4 component) and to identify the instant of occurrence of this component. If the EA4 component is present, this means that the sequencing of atrial contractions is correct because otherwise (i.e., left atrial contractions too late), the EA4 component would be mixed in the component of the EA signal corresponding to the immediately following ventricular contraction (EA1 component). The atrial stimulation interval (AA interval) is then dynamically adjusted depending on the result of this analysis.
However, this technique requires an implantable lead provided with an endocardial acceleration sensor, and a generator capable of processing the EA signals delivered by such a sensor.